The main role of PMN is phagocytosis of bacteria and tissue debri. PMNs are also a major source of cytokines, especially tumour necrosis factor-alpha (TNF-α), and second population that invades the wound consist of macrophages. The function of macrophages is phagocytosis , activation and recruitment of other cells by releasing various cytokines, growth factors such as Vascular endothelial growth Factor, Insulin like Growth Factor and Epidermal Growth Factor. Macrophages regulate matrix synthesis, cell proliferation and angiogenesis.30
Proliferation
Next phase is the proliferation phase spanning from 4-12 days after injury. Tissue continuity is re-established in this phase. The last population of cells invading the wound are Fibroblast and …show more content…
They regress spontaneously within month to years after the initial injury.40 Hypertrophic scars are often red, inflamed, itchy and even painful. They typically appear after burn injury on the trunk and extremities. Hypertrophic scars are frequently misdiagnosed as keloids clinically . Their gross appearance is similar, although keloids grow beyond wound margins.
KELOIDS
Keloids represent a pathological response to cutaneous injury resulting in disfiguring scars with no known satisfactory treatment (Figure 1). Skin injuries such as burns, inflammation, surgery or minor trauma,insect bite induce an overabundant ECM deposition, especially collagen41. Even the spontaneous development of keloids has been discussed 42 but may be the result of a minor, overlooked trauma.
Pathophysiology of keloid A characteristic hallmark of keloids is excessive accumulation of collagen, primarily types I and VI, associated with deposition of other extracellular matrix components, such as fibronectin (Abergel et al., 1985; Peltonen et al., 1991). Collagen accumulation could result either from increased biosynthesis or decreased degradation, and currently a number of modulator molecules interfering with both synthetic and degradative pathways of collagen metabolism in fibroblasts have been recognized (Mauviel and Uitto, …show more content…
VEGF also involved in maintenance of normal adult endothelium, highest expression seen in epithelium adjacent to fenestrated epithelium. Hypoxia is the most important inducer of VEGF through pathways that involves intracellular hypoxia –inducible factor.
VEGF is important in the promotion of neovascularization and cell growth in both normal and pathological wound healing. It serves as an endothelial cell mitogen, increases vascular hyperpermeability, and promotes deposition of an extravascular fibrin matrix. Multiple studies have indicated that VEGF is expressed at higher levels in the underlying dermis, in epidermal keratinocytes, and in capillary lining cells and fibroblasts of keloids in comparison with normal skin.
VEGFs bind to a family of receptor tyrosine kinases (VEGFR-1(FLT1),VEGFR-2( KDR/FLK1),VEGFR-3( FLT 4) . VEGFR-2 is very important for angiogenesis which is highly expressed in endothelium. Antibodies against VEGF are approved for the treatment for several tumours such as renal and colon cancer which require angiogenesis for their spread and
Proliferation
Next phase is the proliferation phase spanning from 4-12 days after injury. Tissue continuity is re-established in this phase. The last population of cells invading the wound are Fibroblast and …show more content…
They regress spontaneously within month to years after the initial injury.40 Hypertrophic scars are often red, inflamed, itchy and even painful. They typically appear after burn injury on the trunk and extremities. Hypertrophic scars are frequently misdiagnosed as keloids clinically . Their gross appearance is similar, although keloids grow beyond wound margins.
KELOIDS
Keloids represent a pathological response to cutaneous injury resulting in disfiguring scars with no known satisfactory treatment (Figure 1). Skin injuries such as burns, inflammation, surgery or minor trauma,insect bite induce an overabundant ECM deposition, especially collagen41. Even the spontaneous development of keloids has been discussed 42 but may be the result of a minor, overlooked trauma.
Pathophysiology of keloid A characteristic hallmark of keloids is excessive accumulation of collagen, primarily types I and VI, associated with deposition of other extracellular matrix components, such as fibronectin (Abergel et al., 1985; Peltonen et al., 1991). Collagen accumulation could result either from increased biosynthesis or decreased degradation, and currently a number of modulator molecules interfering with both synthetic and degradative pathways of collagen metabolism in fibroblasts have been recognized (Mauviel and Uitto, …show more content…
VEGF also involved in maintenance of normal adult endothelium, highest expression seen in epithelium adjacent to fenestrated epithelium. Hypoxia is the most important inducer of VEGF through pathways that involves intracellular hypoxia –inducible factor.
VEGF is important in the promotion of neovascularization and cell growth in both normal and pathological wound healing. It serves as an endothelial cell mitogen, increases vascular hyperpermeability, and promotes deposition of an extravascular fibrin matrix. Multiple studies have indicated that VEGF is expressed at higher levels in the underlying dermis, in epidermal keratinocytes, and in capillary lining cells and fibroblasts of keloids in comparison with normal skin.
VEGFs bind to a family of receptor tyrosine kinases (VEGFR-1(FLT1),VEGFR-2( KDR/FLK1),VEGFR-3( FLT 4) . VEGFR-2 is very important for angiogenesis which is highly expressed in endothelium. Antibodies against VEGF are approved for the treatment for several tumours such as renal and colon cancer which require angiogenesis for their spread and